Effect of reservoir/excess pressure on diastole

As discussed in the brief history of the reservoir-wave hypothesis, the idea of a reservoir pressure was to eliminate the large, self-cancelling forward and backward waves that are inevitably found when the arterial pressure and flow waveforms are separated into their forward and backward components. For reasons detailed elsewhere [link to wia page on wave separation], these waves are very difficult to explain physically or physiologically. Briefly, such self-cancelling waves do exist in systems that exhibit standing waves, but the evidence for standing waves in the aorta is very weak. [link to steady state oscillation]. In the absence of a standing wave, the energy for these waves would have to come form the ventricle, but that is impossible since the valve is closed during diastole.

The figure shows the result of separating the measured pressure (black) into its forward (blue) and backward (red) components. The top graph shows the pressure and the bottom the velocity. The separation is done using wave intensity analysis [link to separation of forward and backward waves] but identical results are obtained if the separation is done using impedance analysis methods first developed by Westerhof and his colleagues [link to Hughes & Parker]. The data are measured in the human ascending aorta. The results demonstrate some very reasonable features. For a brief period at the start of systole the forward pressure is identical to the measured pressure and the backward pressure is zero. This is exactly what would be expected if there was insignificant wave activity in the arteries during late systole. Then the contraction of the ventricle would generate a compression wave that propagated along the aorta. There would be no backward waves until some time later when this initial compression wave was reflected from some reflection site downstream and then travels back to the measurement site. The problem comes in diastole where we see that the forward and backward pressure waveforms are very nearly equal (and the forward and backward velocity waveforms are very nearly equal with opposite signs). As discussed, the only way that this could happen physically is if there was a large standing wave in the arterial system, and that is not consistent with observations. For example, during ectopic or missing beats the pressure continues to fall off exponentially as it does normally during late diastole. If there was a standing wave, we would expect to see some effect of it during the time when the next beat would have occurred. Solving this problem was the motivation for the original work on the reservoir-wave hypothesis.

This figure show the same data in the same format with the measured pressure (black) separated into the reservoir pressure (green) and the excess pressure (not shown) which is further separated into its forward (blue) and backward (red) components. The second graph shows the measured velocity (black) with the separated forward (blue) and backward (red) velocity waveforms. We get a very different picture of the waves when the reservoir pressure is separated out. Note first of all that the problem of physiologically meaningless, self-cancelling forward and backward waves during diastole has disappeared. The reservoir pressure accounts for virtually all of the measured pressure during diastole and so the wave pressure (like the velocity) is effectively zero during diastole. Note also that the magnitude of the forward wave is similar during early systole, which follows because the capacitance-like reservoir pressure follows the sudden increase in pressure during the initial contraction wave only sluggishly. Finally, note that the backward pressure wave is greatly reduced once the reservoir pressure is accounted for.

Here are the two examples side by side to show their differences more clearly:

wave separation without reservoir pressure	wave separation with reservoir pressure

It seems form this, and many other examples, that the reservoir-wave hypothesis may be a useful way to think about arterial mechanics. First we have to define the reservoir pressure more exactly. We will then discuss ways of estimating it from clinical measurements. Only then will we be in a position to interpret the meaning of the reservoir/excess pressure and, more importantly assess how useful it is for interpreting clinical measurements.